For years, scientists have been warning us that a pandemic was all but inevitable. Now it's here, and the rest of us have a lot to learn. Fortunately, science writer Carl Zimmer is here to guide us. In this compact volume, he tells the story of how the smallest living things known to science can bring an entire planet of people to a halt--and what we can learn from how we've defeated them in the past.Planet of Viruses covers such threats as Ebola, MERS, and chikungunya virus; tells about recent scientific discoveries, such as a hundred-million-year-old virus that infected the common ancestor of armadillos, elephants, and humans; and shares new findings that show why climate change may lead to even deadlier outbreaks. Zimmer’s lucid explanations and fascinating stories demonstrate how deeply humans and viruses are intertwined. Viruses helped give rise to the first life-forms, are responsible for many of our most devastating diseases, and will continue to control our fate for centuries. Thoroughly readable, and, for all its honesty about the threats, as reassuring as it is frightening, A Planet of Viruses is a fascinating tour of a world we all need to better understand.
|Publisher:||University of Chicago Press|
|Product dimensions:||5.50(w) x 8.50(h) x 0.40(d)|
About the Author
Carl Zimmer is a columnist for the New York Times, writes for National Geographic and other magazines, and is the author of thirteen books, including Parasite Rex, Soul Made Flesh, and Microcosm. He is also a lecturer at Yale University, where he teaches writing about science and the environment.
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A Planet of Viruses
By Carl Zimmer
The University of Chicago PressCopyright © 2015 The Board of Regents of the University of Nebraska
All rights reserved.
The Uncommon Cold
How Rhinoviruses Gently Conquered the World
Around 3,500 years ago, an Egyptian scholar sat down and wrote the oldest known medical text. Among the diseases he described in the so-called Ebers Papyrus was something called resh. Even with that strange-sounding name, its symptoms — a cough and a flowing of mucus from the nose — are immediately familiar to us all. Resh is the common cold.
Some viruses are new to humanity. Other viruses are obscure and exotic. But human rhinoviruses — the chief cause of the common cold, as well as asthma attacks — are old, cosmopolitan companions. It's been estimated that every human being will spend a year of his or her life lying in bed, sick with colds. The human rhinovirus is, in other words, one of the most successful viruses of all.
Hippocrates, the ancient Greek physician, believed that colds were caused by an imbalance of the humors. Two thousand years later, in the early 1900s, our knowledge of colds hadn't improved much. The physiologist Leonard Hill declared that colds were caused by walking outside in the morning, moving from warm air to cold.
In 1914, a German microbiologist named Walther Kruse gained the first solid clue about the origin of colds by having a snuffly assistant blow his nose. Kruse mixed the assistant's mucus into a salt solution, poured it through a filter, and then put a few drops of the filtered fluid into the noses of twelve colleagues. Four of them came down with colds. Later, Kruse did the same thing to thirty-six students. Fifteen of them got sick. Kruse compared their outcomes to thirty-five people who didn't get the drops. Only one of the drop-free individuals came down with a cold. Kruse's experiments made it clear that some tiny pathogen was responsible for the disease.
At first, many experts believed it was some kind of bacteria. But the American physician Alphonse Dochez ruled that out in 1927. He filtered the mucus from people with colds, using fine filters much as Beijerinck had filtered tobacco plant sap thirty years before. Even with the bacteria removed, the fluid could still make people sick. Only a virus could have slipped through Dochez's filters.
It took another three decades before scientists figured out exactly which viruses had slipped through. The most common of them are known as human rhinoviruses (rhino means nose). Rhinoviruses are remarkably simple, with only ten genes apiece. (Humans have about twenty thousand genes.) And yet their haiku of genetic information is enough to let rhinoviruses invade our bodies, outwit our immune system, and produce new viruses that can escape to new hosts.
Rhinoviruses spread by making noses run. People with colds wipe their noses, get the virus on their hands, and then spread the virus onto doorknobs and other surfaces they touch. The virus hitches onto the skin of other people who touch those surfaces and then slips into their bodies, usually through the nose. Rhinoviruses can invade the cells that line the interior of the nose, throat, or lungs. They trigger the cells to open up a trapdoor through which they slip. Over the next few hours, a rhinovirus will use its host cells to make copies of its genetic material and protein shells to hold them. The host cell then rips apart, and the new virus escapes.
Rhinoviruses infect relatively few cells, causing little real harm. So why can they cause such miserable experiences? We have only ourselves to blame. Infected cells release signaling molecules, called cytokines, which attract nearby immune cells. Those immune cells then make us feel awful. They create inflammation that triggers a scratchy feeling in the throat and leads to the production of a lot of mucus around the site of the infection. In order to recover from a cold, we have to wait not only for the immune system to wipe out the virus, but also for the immune system itself to calm down.
The Egyptian author of the Ebers Papyrus wrote that the cure for resh was to dab a mixture of honey, herbs, and incense around the nose. Fifteen centuries later, the Roman scholar Pliny the Elder recommended rubbing a mouse against the nose instead. In seventeenth-century England, cures included a blend of gunpowder and eggs and of fried cow dung and suet. Leonard Hill, the physiologist who believed a change of temperature caused colds, recommended that children start their day with a cold shower.
Today, there's still no cure for the common cold. The best treatment yet found is zinc, which blocks the growth of rhinoviruses. People who start taking zinc within a day of the start of a cold can shave off a day or more from their illness. Parents often give children cough syrup for colds, but studies show it doesn't make people get better faster. In fact, cough syrup also poses a wide variety of rare yet serious side effects, such as convulsions, rapid heart rate, and even death. The US Food and Drug Administration warns that children under the age of two — the people who get colds the most — should not take cough syrup.
All too often, doctors end up giving antibiotics to their patients with colds. This is a fundamentally pointless treatment, because antibiotics work only on bacteria and are useless against viruses. Doctors sometimes prescribe them because it's not clear whether a patient has a cold or a bacterial infection. In other cases, they may be responding to pressure from worried parents to do something. But antibiotics aren't just useless for colds. They're also a danger to us all, because they help foster the evolution of increasingly drug-resistant bacteria in our bodies and in the environment. Failing to treat their patients, doctors are actually raising the risk of other diseases for everyone.
One reason the cold remains so hard to treat may be that we've underestimated the rhinovirus. It exists in many forms, and scientists are only starting to get a true reckoning of its genetic diversity. By the end of the twentieth century, scientists had identified dozens of strains, which belonged to two great lineages, known as HRV-A and HRV-B. In 2006, Ian Lipkin and Thomas Briese of Columbia University were searching for the cause of flu-like symptoms in New Yorkers who did not carry the influenza virus. They discovered that a third of them carried a strain of human rhinovirus that was not closely related to either HRV-A or HRV-B. Lipkin and Briese dubbed it HRV-C. Since their discovery, researchers have found HRV-C all around the world. From one region to another, the variations in HRV-C's genes are few. Their uniformity suggests that this lineage emerged just a few centuries ago and rapidly spread around the world.
The more strains of rhinoviruses scientists discover, the better they come to understand their evolution. All human rhinoviruses share a core of genes that have changed very little over the centuries. Meanwhile, a few parts of the rhinovirus genome are evolving very quickly. These regions appear to help the virus avoid being killed by our immune systems. When our bodies build antibodies that can stop one strain of human rhinovirus, other strains can still infect us because our antibodies don't fit on their surface proteins. Consistent with this hypothesis is the fact that people are typically infected by several different human rhinovirus strains each year.
The diversity of human rhinoviruses makes them a very difficult target to hit. A drug or a vaccine that attacks one protein on the surface of one strain may prove to be useless against others that have a version of that protein with a different structure. If another strain of human rhinovirus is even a little resistant to such treatments, natural selection can foster the spread of new mutations, leading to much stronger resistance.
Despite this daunting diversity of rhinoviruses, some scientists still think it may be possible to create a cure for the common cold. The fact that all strains of human rhinoviruses share a common core of genes suggests that the core can't withstand mutations. If scientists can figure out ways to attack the rhinovirus's genetic core, they may be able to stop the disease.
One promising target in the rhinovirus core is a stretch of genetic material that folds into a loop shaped like a cloverleaf. Every rhinovirus scientists have studied carries the same cloverleaf structure. It appears to be essential for speeding up the rate at which a host cell copies rhinovirus genes. If scientists can find a way to disable the cloverleaf, they may be able to stop every cold virus on Earth.
But should they? The answer is actually not clear. Human rhinoviruses impose a serious burden on public health, not just by causing colds, but by opening the way for more harmful pathogens. Yet the effects of human rhinovirus itself are relatively mild. Most colds finish in under a week, and 40 percent of people who test positive for rhinoviruses suffer no symptoms at all. In fact, human rhinoviruses may offer some benefits to their human hosts. Scientists have gathered a great deal of evidence that children who get sick with relatively harmless viruses and bacteria may be protected from immune disorders when they get older, such as allergies and Crohn's disease. Human rhinoviruses may help train our immune systems not to overreact to minor triggers, instead directing their assaults to real threats. Perhaps we should not think of colds as ancient enemies but as wise old tutors.CHAPTER 2
Looking Down from the Stars
Influenza's Never-Ending Reinvention
Influenza. If you close your eyes and say the word aloud, it sounds lovely. It would make a good name for a pleasant, ancient Italian village. Influenza is, in fact, Italian (it means influence). It is also, in fact, an ancient name, dating back to the Middle Ages. But the charming associations stop there. Medieval physicians believed that stars influenced the health of their patients, sometimes causing a mysterious fever that swept across Europe every few decades. Influenza has continued to burden the world with periodic devastation. In 1918, a particularly virulent outbreak of the flu infected 500 million people — a third of humanity at the time — and killed an estimated 50 million people. Even in years without an epidemic, influenza takes a brutal toll. The World Health Organization estimates that each year the flu infects 5 to 10 percent of all adults and 20 to 30 percent of all children. Somewhere between a quarter and half a million people die of the flu each year.
Today scientists know that influenza is the work not of the heavens, but of a microscopic virus. Like cold-causing rhinoviruses, influenza viruses manage to wreak their harm with very little genetic information — just thirteen genes. They spread in the droplets sick people release with their coughs, sneezes, and runny noses. A new victim may accidentally breathe in a virus-laden droplet or pick it up on a doorknob and then bring now-contaminated fingers in contact with the mouth. Once a flu virus gets into the nose or throat, it can latch onto a cell lining the airway and slip inside. As flu viruses spread from cell to cell in the lining of the airway, they leave destruction in their wake. The mucus and cells lining the airway get destroyed, as if the flu viruses were a lawn mower cutting grass.
When healthy people get infected by influenza viruses, their immune systems can launch a counterattack in a matter of days. In such cases, the flu causes a wave of aches, fevers, and fatigue, but the worst of it is over within a week. In a small fraction of its victims, the flu virus opens the way for more serious infections. Normally, the top layer of cells serves as a barrier against a wide array of pathogens. The pathogens get trapped in the mucus, and the cells snag them with hairs, swiftly notifying the immune system of intruders. Once the influenza lawnmower has cut away that protective layer, pathogens can slip in and cause dangerous lung infections, some of which can be fatal.
There are still paradoxes to influenza's effects that virologists don't understand. Seasonal flu is most dangerous for people with weak immune systems — particularly young children and the elderly — because they can't keep the virus in check. But in the 1918 outbreak, it was young adults — people with strong immune systems — who proved to be particularly vulnerable. One theory holds that certain strains of the flu provoke the immune system to respond so aggressively that it ends up devastating the host instead of wiping out the virus. But some scientists doubt this explanation and think the true answer lies elsewhere. It's possible, for example, that in 1918, older people carried protective antibodies from a similar pandemic in 1889.
While the effects of the flu may still be mysterious, its origins are clear. It came from birds. Birds carry all known strains of human influenza viruses, along with a vast diversity of other flu viruses that don't infect humans. Many birds carry the flu without getting sick. Rather than infecting their airways, flu viruses typically infect the guts of birds; the viruses are then shed in bird droppings. Healthy birds that ingest the virus-laden water become infected in turn.
Sometimes a strain of bird flu will end up in people. They may work on a chicken farm, or butcher poultry in a market. A bird flu virus that ends up in a human airway may seem out of place. But it turns out the receptors on cells in bird guts are similar in shape to those in our airways. Bird flu viruses can sometimes latch onto those receptors and slip inside.
But the transition from bird to human is not a simple one. The genes a bird flu virus needs to thrive are different from those needed inside a human body. Human bodies are cooler than bird bodies, for example, and that difference means that molecules need different shapes to run efficiently.
As a result, bird flu viruses that leap into humans usually wind up in viral dead ends because they can't spread from person to person. Starting in 2005, for example, a strain of flu from birds called H5N1 began to sicken hundreds of people in Southeast Asia. It proved to be much deadlier than ordinary strains of seasonal flu, and so public health workers tracked it closely, taking measures to halt its spread. But year in and year out, it never showed any ability to move from one human to another. H5N1 viruses that wound up in people always died out — either because their hosts destroyed them, or because they killed their hosts.
But every now and then, bird flu viruses adapt to our bodies. Each time they replicate, the new viruses contain genetic mistakes known as mutations. Some of the mutations have no effect on viruses. Some leave them unable to reproduce. But a few mutations give flu viruses a reproductive advantage.
Natural selection favors these beneficial mutations. Some help the virus by altering the shape of the proteins that stud the virus shell, allowing them to grab human cells more effectively. Others help them spread from person to person.
Once a flu strain gets established in humans, it can spread around the world and begin to pulsate in a seasonal rise and fall. In places like the United States, most flu cases occur during the winter. According to one hypothesis, this is because the air is dry enough in those months to allow virus-laden droplets to float in the air for hours, increasing their chances of encountering a new host. At other times of the year, the humidity causes the droplets to swell and fall to the ground.
When a flu virus hitches a ride aboard a droplet and infects a new host, it sometimes invades a cell that's already harboring another flu virus. And when two different flu viruses reproduce inside the same cell, things can get messy. The genes of a flu virus are stored on eight separate segments, and when a host cell starts manufacturing the segments from two different viruses at once, they sometimes get mixed together. The new offspring end up carrying genetic material from both viruses. This mixing, known as reassortment, is a viral version of sex. When humans have children, the parents' genes are mixed together, creating new combinations of the same two sets of DNA. Reassortment allows flu viruses to mix genes together into new combinations of their own.
A quarter of all birds with the flu have two or more virus strains inside them at once. The viruses swap genes and gain new adaptations, such as the ability to move from living in wild birds to chickens, or even to mammals such as horses or pigs. And sometimes, on very rare occasions, reassortment can combine genes from avian and human viruses, creating a recipe for disaster. The new strain that results from this combination can easily spread from person to person. And because it has never circulated among humans before, no one has any defenses that could slow the new strain's spread.
Once bird flu viruses evolve into human pathogens, they continue to swap genes among themselves. This ongoing reassortment allows the viruses to escape destruction. Before people's immune systems get too familiar with a flu strain's surface proteins, it can use a little viral sex to take on a new disguise.
Excerpted from A Planet of Viruses by Carl Zimmer. Copyright © 2015 The Board of Regents of the University of Nebraska. Excerpted by permission of The University of Chicago Press.
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Table of Contents
Foreword by Judy Diamond and Charles Wood INTRODUCTION “A Contagious Living Fluid” Tobacco Mosaic Virus and the Discovery of the Virosphere OLD COMPANIONS The Uncommon Cold How Rhinoviruses Gently Conquered the World Looking Down from the Stars Influenza’s Never-Ending Reinvention Rabbits with Horns Human Papillomavirus and Infectious Cancer EVERYWHERE, IN ALL THINGS The Enemy of Our Enemy Bacteriophages as Viral Medicine The Infected Ocean How Marine Phages Rule the Sea Our Inner Parasites Endogenous Retroviruses and Our Virus-Riddled Genomes THE VIRAL FUTURE The Young Scourge Human Immunodeficiency Virus and the Animal Origins of Diseases Becoming an American The Globalization of West Nile Virus Predicting the Next Plague Ebola Virus and the Many Others Like It The Long Goodbye The Delayed Oblivion of Smallpox EPILOGUE The Alien in the Water Cooler Giant Viruses and the Definition of Life Acknowledgments Selected References Credits Index